VCAM1Vascular Cell Adhesion Molecule 1
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Expression levels of PSGL1, ICAM1, and VCAM1 did not significantly differ between nasal polyps and inferior turbinates (Figure 1).
Analysis of the 10 candidate genes (Tph2, Sspo, Ptprq, Pole, CXCR4, PLLP, TNFSF4, VCAM1, SLC8A2, and SLC7A11) with GeneMANIA and Cytoscape revealed interactions among them (Figure 5), with the corresponding functions of these genes being predominantly related to immune responses (see the following list).
However, a significant association between age and VCAM-1 independent of the cardiovascular risk was shown, and others also found VCAM1 elevated in plasma of AD cases [43], which is consistent with our findings.
The fibrates, gemfibrozil, and fenofibrate are also used as PPAR[alpha] agonists which limit cytokine-induced induction of the inflammatory functions of VCAM1 in response to TNF-[alpha] and tissue factor gene expression [117].
One week after AMI, [Adipoq.sup.-/-] mice displayed a reduction in the number of BM-residing and circulating angiogenic cells, coinciding with a downregulated gene expression of the chemotactic factors Cxcl12 and Ccl5, and the vascular adhesion molecules Icam1 and Vcam1. The decreased BM reserve, mobilization and homing capacity of CACs could be important factors contributing to the decreased neovascularization capacity that was observed under adiponectin deficient conditions.
The results show that the VCAM1 expression was significantly upregulated after 24 h of PM exposure in the absence of T cells, compared to the control (22.4% [+ or -] 1.9% versus 0.42% [+ or -] 0.12%; P < 0.01; Figures 3(a) and 3(b)).
The experimental models studied showed different expression patterns of NF-kB and VCAM1. This result was previously reported by our laboratory [18].
Since we had the availability of the hemodynamic measurements performed into the venous segments that were surgically ablated and from which we derived pure vein endothelial cultures (Table 1), in this study we have performed a set of correlation analyses between key in vitro biological characteristics of VEC (spontaneous cell migration, proliferation index and baseline expression levels of ICAM-1, VCAM1, OPG, and TRAIL) and the two major hemodynamic parameters resistance index (RI) and reflux time (RT) (Table 2).
Several inflammatory mediators have been implicated in the pathogenesis of cardiovascular disorders (CVD) [1] and most of them, such as the flogistic molecules CD40 and its soluble ligand, the adhesion molecules ICAM-1, VCAM1, E-selectin and P-selectin, the peptides NT-proBNP and troponin T, and fibrinogen, are useful as systemic biomarkers for inflammation and tissue damage associated with CVD [2, 3].
Estos estimulos permiten la liberacion de la subunidad inhibitoria (42), posibilitando la translocacion del NF[kappa]B al nucleo para promover la transcripcion de genes como el del factor tisular, las moleculas de adhesion celular (molecula de citoadhesion vascular 1 (VCAM1), molecula de adhesion intercelular 1 (ICAM-1) y selectina-E), el gen del receptor del tromboxano y citoquinas proinflamatorias como IL-1; IL-2, IL-6, IL-8, TNF-[alfa] e INF[gamma] (42, 44, 45).
Previous study suggested that many genes and signalling pathway are involved in early pregnancy, and some genes are essential for maintaining pregnancy, and the miscarriage was triggered by the dysfunction of these genes, such as cadherin 2 (CDH2), which is a gene of cell adhesion molecules (CAMs) [5]; collagen type VI alpha 3 chain (COL6A3), thrombospondin 1 (THBS1), fibronectin 1, integrin beta 4 (ITGB4) [6], which are all PI3KAkt signaling pathway genes; matrix metallopeptidase 14 (MMP14), vascular cell adhesion molecule 1 (VCAM1) [7], matrix metallopeptidase 9 (MMP9), which are all tumor necrosis factor (TNF) signaling pathway genes; additionally, MAPK signaling pathway [8] and Hippo signaling pathway [9] are involved in maintaining pregnancy.
Primary antibodies against [beta]-actin and vascular cell adhesion molecule 1 (VCAM1) and appropriate secondary antibodies were procured from Santa Cruz Biotechnology, Inc.